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155 Cards in this Set
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pH = 7.33 Bicarbonate = 14 pCO2 = 28 |
Metabolic Acidosis low bicarb so low pCO2 so it is compensating correctly |
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pH = 7.46 Bicarbonate 14 pCO2 = 20 |
Respiratory Alkylosis low pCO2 so low bicarb so it is compensating correctly
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pH =3.74 Bicarbonate = 19 pCO2 = 34 |
Metabolic Acidosis low bicarb so low pCOs so it is compensating correctly |
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pH = 7.47 Bicarbonate = 34 pCO2 = 47 |
Metabolic Alkylosis bicarb is high so pCO2 is high this is compensating correctly |
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pH = 7.07 Bicarbonate = 14 pCO2 = 47 |
Acidosis, but bicarb is low and pCO2 is high so this is MIXED |
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pH = 7.40 Bicarbonate = 12 (24) pCO2 = 20 (40) |
Mixed
the bicarb is low which suggests |
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Type B Intercalated Cells |
secrete base saves acid |
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compensation in metabolic acidosis |
decrease CO2 hyperventilate |
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compensation in metabolic alkalosis |
increase CO2 hypoventilating |
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compensation in respiratory acidosis |
increase bicarbonate secrete less bicarbonate |
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compensation in respiratory alkalosis |
decrease bicarbonate secrete more bicarbonate via beta-intercalated cells |
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Anion Gap Equation |
Na - (Cl + HCO3) |
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sodium= 140 bicarbonate= 24 chloride = 105
Anion Gap |
140 - (24+105) Anion Gap = 11 |
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Anion Gap Mnemonic (AG increased) |
GOLD MARK
Glycol, Oxoproline, Lactate, D-Lactate, Methanol, Aspirin, Renal Failure, Ketoacidosis |
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Anion Gap Decreased Differential |
Diarrhea or Renal Tubular Acidosis |
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where do loop diuretics work and give an example |
thick ascending limb of the loop of Henle
Furosemide |
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what is the mechanism of action of loop diuretics |
blocks the Na-K-2Cl cotransporter in the thick ascending limb of Henle's loop
this leads to a dissipation of the medullary gradient and a profound diuresis and excretion of all electrolytes |
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which diuretics are Potassium losing |
Manitol Furosemide (ascending limb) Thiazides (DCT) |
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which diuretics are potassium saving |
spironolactone and triamterene |
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what type of AKI is suggested when few hyaline casts are present |
prerenal- makes sense because the tubule itself is not affected |
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what type of AKI is suggested when proteinuria and casts are present |
-ATN- mild to moderate proteinuria, pigmented granular casts
-AIN- mild to moderate proteinuria, leukocytes, WBC casts, eosinophils
-Acute GN- moderate to severe proteinuria, RBC, RBC casts
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what kind of AKI is suggestive when there is no proteinuria and no hyaline casts |
postrenal- no casts make sense, the nephrons aren't affected so we wouldn't expect lots of protein to be lost |
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what factors will give you a falsely low FeNa and what does this inacurrately suggest? |
contrast agents cause intense vasoconstriction
acute glomerulonephritis causes vascular inflammation |
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what do shrunken kidneys on ultrasound suggest |
chronic intrinsic kidney disease |
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in the case of type 1 DM, what symptom suggests another condition while the converse is not true |
those with nephropathy have retinopathy while the converse is not necessarily true. |
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what leads to the formation of calcium oxalate crystals |
ethylene glycol
have the X structure |
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what pain medicine should be given for stone disease |
Ketorolac
Ofirmev (less effective)
try these before using a narcotic |
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what medications are recommended for people with stones |
pain meds- ketorolac IV fluids and antiemetic (zofran) antibiotics alpha blockers (flomax) strainer |
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why give an alpha blocker to someone with stones |
it improves the spontaneous stone passage rate |
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almost all calcium stones start from what? |
Randall's plaques, which are always calcium phosphate |
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what are Randall's plaques made of and what do they lead to? |
calcium phosphate
they lead to most calcium stones |
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what is the metabolic workup on someone with kidney stones (this may actually be screening for someone at risk for kidney stones) |
serum BMP (with calcium) serum Mg, Phosphate, Uric acid Intact PTH and Vitamin D 24 hour urine |
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what is the order of the renal hilum form anterior to posterior |
renal vein --> renal artery --> renal pelvis |
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what is the blood supply of the bladder |
superior, middle, and inferior vesical arteries off the internal iliac (hypogastric) |
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describe the innervation of the bladder |
sympathetic- storage (relaxes bladder and tightens sphincter) (Hypogastric nerve from T11-L2)
parasympathetic- voiding (pelvic nerve from S2-S4 sacral plexus)
somatic- voluntary control of the external sphincter and pelvic floor muscles (pudendal nerve from S2-S4 sacral plexus) |
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what nerves allow for voiding |
parasympathetic- voiding (pelvic nerve from S2-S4 sacral plexus)
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what is the innervation for voluntary bladder control |
somatic- voluntary control of the external sphincter and pelvic floor muscles (pudendal nerve from S2-S4 sacral plexus) |
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what condition is assocaited with sterile pyuria |
Tuberculosis stones cancer |
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treatment for simple UTI |
3 days on sulfa/trimethoprim or nitrofurantoin |
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treatment for complicated UTI |
7-14 days of cipro and possibly urology referral change catheter if they have one |
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what medication is given as a night time dose prophylactically for UTI |
nitrofurantoin or TMP for 9-12 months |
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how do we treat purple urine
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if asymptomatic- treat their constipation and change the foley catheter
if symptomatic- treat their constipation and give an antibiotic |
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what bacteria is associated with urease stones |
proteus |
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which bacteria does not produce urease |
E. Coli |
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what drug is used to inhibit urease production |
lithostat
acetohydroxamic acid
we probably don't have to know this |
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how do we treat uric acid stones |
if serum uric acid is normal- potassium citrate to alkalinize the urine (because we have high urinary acid levels)
if serum uric acid id high- also add allopurinol |
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which crystals look like an envelope |
triple phosphate |
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describe the pathogenesis of diabetic neuropathy |
the afferent arteriole dilates which increases the GFR and increases the hydrostatic pressure.
can be treated with ACEI, ARB, low protein diet, decreased BP |
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what should all diabetics be given |
ACEI or ARB |
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what do Kimmelstiel-Wilson nodules suggest |
DN in type 1 or type 2 diabetes |
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what do diffuse granular lesions in the glomerulus suggest |
Diabetic neuropathy esp in type 1 diabetes |
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compare insipient to overt DN |
insipient- microalbuminuria 30-300 mg/24 hours
Overt- Macroalbuminuria >300 mg/24 hours hypertension and relentless decline in GFR persistent albuminuria |
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microalbuminuria in the context of type 1 and type 2 |
type 1- micro... predicts the development of diabetic nephropathy
type 2- micr... is associated with cardiovascular mortality |
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what is the most common systemic or secondary etiology for nephrotic syndromes |
diabetic nephropathy |
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what is the target blood pressure in people with diabetic kidney disease |
130/80 |
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what is ramipril |
it significantly reduced the rate of stroke, heart attack, and death in people with DM
it is an ACEI |
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what is the major cause of death in people with ESRD |
cardiovascular disease |
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what condition presents with: - large subendotheial deposits - mesangial deposits - fibrin thrombi |
lupus glomerulonephritis |
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describe stage 2 of lupus GN |
mesangial GN |
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describe stage 3 of lupus GN |
focal proliferative GN |
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what is suggested by the presence of wire loop deposits |
Diffuse proliferative lupus GN (class 4)
lupus until proven otherwise |
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what condition is nephrotic with widespread BM thickening and subepitheial deposits |
Membranous Lupus GN (Class 5)
the subepithelial deposits are the membranous humps |
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a patient comes in with purpuric skin lesions on their buttocks with abdominal pain, athralgia, and renal abnormalities |
Hencoh-Schonlein Purpura
systemic disease- vasculitis involving IgA |
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what condition involves effacement of the foot processes |
minimal change (lipoid) focal segmental glomerulosclerosis
both are nephrotic |
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nodular hyaline masses within a globule of the glomerulus |
nodular glomerulosclerosis in DM
Kimmelstiel-Wilson's disease |
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what condition produces anti-GBM antibodies |
Goodpastures |
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what are the four types of tubulointerstitial disease |
ischemic toxic infectious/inflammatory stones |
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patchy necrosis of tubular epithelial cells due to shock and poor perfusion of the kidney reversible if caught in time |
"ischemic" acute tubular necrosis |
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if the tubules are damaged by a toxin what part of the tubule is primarily affected? |
proximal tubule |
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describe the patters of tubular damage in ischemic and toxic ATN |
ischemic- it is patchy, a little bit here and there
toxic- PCT, descending limb of loop of henle
there are casts in both everywhere after the ascending limb
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what condition can lead to thyroidization of the kidney |
chronic pyelonephritis
thyroidization is called atrophic dilated tubules |
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when would we see sterile pyuria |
TB |
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what is significant about polyoma virus pyelonephritis |
it manifests itself in transplants-immunosuppression |
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a patient had tennis elbow, took NSAID's, and developed renal failure. What is the problem |
acute drug induced tubulointerstitial nephritis
also seen in penicillins and diuretics |
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chronic tubulointerstitial nephritis |
caused by chronic analgesic abuse (acetaminophen)
leads to chronic renal failure due to atrophy of the nephrons and interstitial fibrosis |
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a patient produces proteins. these proteins combine with tamm-horsfall protein to form complexes that damage the kidney |
myeloma kidney |
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patient has cysts in the liver, spleen, kidneys and liver |
AD polycystic kidney disease |
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multiple cyatic dilations of collecting ducts in the medulla |
renal medullary cysts
(medullary sponge kidney) |
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Nephronophthisis |
medullary cystic complex- cyst at the corticomedullary junction |
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nephrocalcinosis |
hypercalcemia leads to tubular cell destruction due to blockage and breakdown of the tubules |
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what kind of stone is proteus associated with |
triple stones- magnesium, ammonium, phosphate |
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what are the 4 main types of stones |
-calcium oxalate or phosphate -triple stones (magnesium, ammonium, phosphate (caused by proteus) -uric acid stones -cystine |
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the mesonephros becomes what? |
the mesonephric duct which contributes to the ductus deferens |
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what is the most common site of obstruction (hydronephrosis) in a fetus |
ureteropelvic junction- it is the most narrow |
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what is used to measure effective renal plasma flow |
PAH (para-aminohippuric acid) because it is actively secreted in the proximal tubule
it underestimates the true renal plasma flow by 10% |
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what is the effect of NSAIDs on the glomerulus |
prostaglandins dilate the afferent arteriole increased renal plasma flow and GFR
NSAID's stop this from happening |
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what is the effect of an ACEI on the glomerulus |
angiotensin 2 preferentially constricts the efferent arteriole decreasing renal plasma flow and increasing GFR.
ACEI stop this from happening |
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filtered - excreted |
reabsorption |
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excreted - filtered |
secreted |
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Bartter syndrome |
reabsorptive defect in thick ascending loop of Henle
hypokalemia and metabolic acidosis WITH hypercalciuria
"barter away all your pot" low K |
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Gitelman Syndrome |
hypokalemia and metabolic acidosis WITHOUT hypercalciuria |
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african american or hispanic with effacement of podocyte foot processes
child with effacement of podocyte foot processes |
1. Focal segmental glomerulosclerosis
2. Minimal change disease (lipoid nephrosis) |
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congo red stain shows apple-green birefringence under polarized light
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Amyloidosis
"kingdom of amylor takes place in the congo near an apple tree" |
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Nephrotic Syndromes (x6) |
1. Minimal chnage 2. Focal Segmental GS 3. Membranous nephropathy 4. Amyloidosis 5. Membranoproliferative GN 6. Diabetic GlomeruloNEPHROPATHY |
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GBM thickening with tram-track appearance due to subendothelial immune complex formation |
Type 1- Membranoproliferative GN (nephrotic)
"the train track is proliferating"
associated with HBV and HCV |
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GBM thickening due to C3 nephritic factor |
Type 2- Membranoproliferative GN
nephrotic syndrome |
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patient presents with Kimmelstiel-wilson lesions and GBM thickening |
Diabetic glomerulonephropathy (nephrotic syndrome) |
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Nephritic Syndromes (x5) |
1. Acute poststreptococcal glomerulonphritis 2. RPDN a. Goodpasture's 3. Diffuse proliferative glomerulonephritis 4. IgA nephropathy (Berger Disease) 5. Alport Syndrome |
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patient presents with cola colored urine, hypercellular glomeruli, starry sky and lump bumpy on IF, subepithelial immune complex humps |
acute poststreptococcal GN (nephritic) |
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patient presents with crescents composed of fibrin and macrophages, hematuria, red cell casts, and antibodies against GBM |
Goodpasture Syndrome (Nephritic) |
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patients presents with mesangial proliferation |
IgA Nephropathy |
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antibodies directed against the alpha-3 chain of collagen |
Goodpasture's Syndrome
Nephritic syndrome- RPGN |
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GN, deafness, thinning of the glomerular BM
defect in alpha 5 chain of type 4 collagen |
Alport Syndrome (nephritic) |
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In what condition do we become hypercoagulable due to a loss of albumin |
Nephrotic syndrome- we lose albumin (elads to edema), lose Ig (leads to increased risk of infection, lose AT 3 (hypercoagulable) |
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mesangial proliferation |
IgA Nephropathy (nephrotic) |
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patient presents with granular IF, thick basement membrane, subepithelial deposits. patient has Hep C |
Membranous Nephropathy (nephrotic)
granular IF means immune complex deposition. "spike and done appearance"
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Thickening BM and tram-track appearance |
Membranoproliferative GN (nephrotic) |
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which nephrotic syndrome contains:
1. Subepithelial deposits 2. Intramembranous deposits 3. Subendothelial deposits |
1. Membranous GN 2. Type 2 MPGN 3. Type 1 MPGN |
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Groups of 2:
1. Effacement of Foot Processes 2. Immune Complex Deposition (Granular IF) 3. Systemic Disease
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1. Minimal Change Disease and FSGN 2. Membranous GN and MPGN 3. Diabetic Nephropathy and Amyloidosis |
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which drugs are Na Cl co-transporter blockers |
thiazides, which work on the distal convoluted tubule |
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which drugs are Na-K-2Cl co-transporter blockers |
Loop Diuretics, which work on the ascending loop of the Loop of Henle |
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which diuretics decrease the risk of developing stones |
thiazide diuretics because they increase the reabsoption of Ca, removing it from the kidney |
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what is one condition we will treat with a thiazide diuretic |
nephrogenic diabetes insipidus |
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how do we treat nephrogenic diabetes insipidus |
adequate water intake
thiazide diuretic |
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what is the most common cause of nephrogenic diabetes insipidus |
Li therapy |
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what can long term lithium therapy lead to |
nephrogenic diabetes insipidus |
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what is a treatment for central diabetes insipidus |
desmopressin- as a V2 agonist it makes the nephron think ADH is present |
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what are the major ions of ICF
major ions of ECF |
ICF: K and Mg; protein and organic phosphates
ECF: Na; Cl and Bicarbonate
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what form of azotemia has an increased BUN/creatinine ratio |
Prerenal and postrenal azotemia
it is decreased in ATN or |
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where is glucose reabsobed |
the proximal tubule via Na-glucose cotransporters |
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compare excretion of a weak acid in acidic urine and alkaline urine |
acidic urine the acid becomes HA (lipid soluble) and is able to back diffuse- decreasing excretion
alkaline urine reduces back diffusion- increasing excretion |
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compare excretion of a weak base in acidic urine and alkaline urine |
acidic urine the base becomes BH (not lipid soluble) and is not able to back diffuse- increasing excretion
alkaline urine increases back diffusion- decreasing excretion |
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patient presents with flank pain that radiates to groin and patient is constantly moving. |
kidney stone |
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patient presents with flank pain that radiates to groin, slight fever, and WBC in urine |
Pyonephrosis
MEDICAL EMERGENCY
they cannot leave without antibiotic and call urology |
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what drug is great at treating pain in kidney stones |
Ketorolac
"KOTOR- Colton loves video games" |
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what drugs are given for kidney stones |
Ketorolac (NSAID) Zofran- antiemetic Flomax- alpha blocker (improves spontaneous passage of stone) Antibiotic |
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alkaline urine leads to the formation of what kind of stone |
triple phosphate (Mg, ammonium, phosphate) |
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proteus infection increases risk of what kind of stone |
triple phosphate (Mg, ammonium, phosphate) |
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which stone is treated with potassium bicarbonate |
uric acid stone to alkalinize the urine and breakdown the stone |
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a stone is radioluscent, what is it |
uric acid stone |
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what is not a factor in determining whether a patient needs to be admitted for a stone |
Hydronephrosis |
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what is ESWL |
extracorporeal shock wave lithotripsy
uses shock waves to break stones into small fragments
used on stones <2.5 cm |
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autonomic dysreflexia |
sudden high blood pressure in spinal cord injury (above T6).
treatment- remove foley, check bladder, emergency nitrate (sodium nitroprusside) |
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GN treated with steroids |
Minimal Change Disease |
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patient presents with periorbital edema |
PSGN: starry sky lumpy bumpy humps granular IF |
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wire looping |
Diffuse Proliferative GN (DPGN)
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Kimmelstiel-Wilson lesions |
Diabetic Glomerulonephropathy |
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congo red stain- apple green biregringence |
amyloidosis (nephrotic) |
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loss of 3p (VHL) tumor suppressor genes |
Renel Cell Carcinoma |
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what is the most common site in the cause of hydronephrosis in infants |
Ureteropelvic junction |
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bladder adenocarcinoma |
came from patent urachus |
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honeymoon cystitis |
women actually a urethritis associated with recent sexual intercourse |
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cystitis glandularis |
inward growth of transitional epithelium with formation of cysts lined by urothelium |
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polypoid cystitis |
chronic irritation of bladder mucosa associated wit indwelling catheters |
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malakoplakia |
form of chronic cystitis caused by e. coli or proteus in people with defect in macrophage function |
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schistosomiasis increase the risk of what type of cancer |
squamous cell carcinoma
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squamous cell carcinoma of the bladder is associated with what |
schistosomiasis |
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WAGR |
Willms tumor Aniridia Genital Abnormalities Retardation |
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A- 3 year old boy presents with hematuria and hypertension. palpable flank mass is present.
B- Boy has mental retardation, Aniridia, Genital abnormalities |
WT1 Mutation
A- Wilms Tumor
B- WAGR |
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mutation in VHL (p3) tumor suppressor gene |
renal cell carcinoma |
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left sided varicocele |
renal cell carcinoma of the left kidney |
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Von Hippel Lindau Disease |
Renal Cell Carcinoma
"Hippo named RC" |
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linear IF |
Goodpasture's |
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Granular IF |
Membranous GN Membranoproliferative GN PSGN*
immune complex means we have granular IF |
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Benign tumor from intercalated cells of the collecting duct.
mahogany brown |
oncocytoma |
